Transcript Respiratory System

Respiratory System
Lecture 2
Gas Exchange & Regulation
Gas Exchange
• occurs between blood &
alveolar air
• across respiratory
membrane
• by diffusion due to
concentration gradient
– differences between O2 & CO2
concentrations
– measured by partial pressures
• greater difference in partial
pressuresgreater rate of
diffusion
• need to understand partial
pressures & diffusion of
gases into & out of liquids to
understand gas exchange
Dalton’s Law of Partial Pressure
• air-mixture of gases & water vapor
• consists of N2-78%-most abundant, O2-20.9%water, CO2,
Argon
• atmospheric pressure is result of collision of all gas
molecules
• at any time 78.6% of collisions involve N2 & 20.9% involve
O2
• each gas contributes to total pressure in proportion to its
relative abundance-Dalton’s Law
• PressureTotal = Pressure1 + Pressure2 ... Pressuren
• pressure contributed by one gas is partial pressure
• directly proportional to % of gas in mixture
• all partial pressures added = total pressure exerted by gas
mixture =760mm Hg
• PN2-parital pressure nitrogen = 78.6 X 760 mm Hg-597 mm
Hg
• PO2 20.9 X 760 = 159 mm Hg
Henry’s Law
• at a given temperature,
amount of gas in solution
is directly proportional
to partial pressure (pp) of
gas
• when gas mixture is in
contact with liquid, each
gas dissolves in
proportion to its partial
pressure
• actual amount in solution
at given pp depends on
solubility of that gas in
that liquid
Partial Pressures in Alveoli &
Alveolar Capillaries
•
•
•
•
•
•
•
•
•
•
•
•
•
oxygen diffuses from alveolar air (PP is
105mm Hg) into blood in pulmonary capillaries
where PO2 is 40 mm Hg
when O2 is diffusing from alveolar air into
deoxygenated blood CO2 is diffusing in
opposite direction
PCO2 of deoxygenated blood is 45 mm Hg
PCO2 of alveolar air-40 mm Hg
CO2 diffuses from deoxygenated blood into
alveoli
left ventricle pumps oxygenated blood into
aorta & through systemic arteries to systemic
capillaries
exchange of O2 & CO2 between systemic
capillaries & tissues cells
PO2 of blood in systemic capillaries is 100
mmHg
in tissue cells it is 40mm Hg
as oxygen diffuses out of capillaries into
tissues carbon dioxide diffuses in opposite
direction
PCO2 of cells is 45 mm Hg
it is 40mm Hg systemic capillary blood
Diffusion at Respiratory Membrane
• efficient
• large PP differences
across membrane
– larger PPfaster
diffusion
• capillary & alveolar
membranes are fused
distances for diffusionsmall
• gases are soluble in lipidpass through surfactant
layer easily
• surface area is huge
Gas Transport
• Major function of blood
• O2
• Co2
Oxygen Transport
• dissolved in
plasma
– normal PO2 of
alveoli, 100ml of
blood contains
0.3ml of O2
• carried in RBC
bound to
hemoglobin
Hemoglobin
• 4 subunits
•
•
•
•
•
•
– 2 & 2ß globular
protein chains
each has one heme
group
each heme has one iron
each Fe can bind one O2
every Hb can carry 4 O2s
there are 280 X 106 Hb
molecules/RBC
each RBC could carry
billion O2 molecules
•
•
•
•
•
Oxyhemoglobin
Hb + O2 HbO2oxyhemoglobin
reversible
Fe-O2 bond-weak
easily broken
without altering
either Hb or O2
• HbO2 O2 + Hb
• deoxyhemoglobin
Amount of Oxygen Bound to HB
• PO2 of plasma
• most important factor determining
how much O2 binds to Hb
• actual amount bound/maximum
that could bind = % saturation
• all binding sites occupied-100%
saturation
Oxyhemoglobin Dissociation Curve
• plots %
saturation Hb
(number of O2
bound) against
PO2
–relates
saturation of Hb
to PP of O2
•
•
•
•
HbO2 Dissociation Curve
not linear-S-shaped
steep slope-flattens or plateaus
shape due to subunits of Hb
each time Hb binds one O2
shape changes slightly
increases ability of Hb to bind
another O2
• when PO2 is between 60 100mmHG, Hb is 90% or more
saturated with oxygen
• blood picks up nearly full load
of O2 from lungs even when
PO2 alveolar air is as low as
60mmg Hg
• increasing PO2 above 80mm Hg
adds little to O2 content of blood
• PO2 < 50 mm, small drops in PO2
cause large release of O2
Importance of Oxyhemoglobin
Dissociation Curve
• shape of Hb saturation curve
extremely important
• over steep initial slopevery small
decreases in PO2 results in very
large changes in amount of O2
bound or released from Hb
• ensures near normal O2 transport
even when O2 content of alveolar
air decreases (important at high
altitudes)
• slope of curve allows blood to
have high O2 content at fairly low
PO2s
• PO2 can fall considerably-without
greatly reducing oxygen supply
Factors Affecting Affinity of O2 & Hb
• various factors increase or
decrease affinity (tightness of
bond) of Hb to O2
• factors will shift curve to left
(higher affinity) or to right
(lower affinity)
• left-more O2 is bound than
released
• right-more O2 is released
than bound
• pH
• pCO2
• temperature
• BPG
Hb & pH
• as pH decreases
shape of Hb
changesreleases O2
more readilyslope of
curve changes
saturation decreases
• more O2 released
• curve shifts to right
• effect of pH on Hb
saturation is Bohr
Effect
Bohr Effect
• Hb acts as buffer for H+
• when H+ bind to amino acids in
Hb
• they alter its structure slightly
decreasing its oxygen carrying
capacity
• increased H+ ion concentration
causes O2 to unload from Hb
• binding of O2 to Hb causes
unloading of H+ from Hb
• elevated pH (lowered H+)
increases affinity of Hb for O2
• shifts O2-Hb dissociation curve
to left
Hb & Temperature
• higher temperature
–curve shifts to
right
–unloading of O2
from Hb is
increased
• lower temperatures
–curve shifts to left
–O2 binds more to
Hb
Hb & Carbon Dioxide
• increase in CO2
– shifts curve to
right
• more O2
released
• decrease in CO2
– shifts curve to
left
• more O2
bound
Hb & BPG
• BPG-2,3 biphosphoglycerate
– produced by RBC during
glycolysis
• higher levels
– unloading of oxygen
increased
– shifts to right
• BPG decreases
– curve shifts to left
– more oxygen is bound
• amount of BPG generated
drops as RBCs age
• BPG drops too lowO2
irreversibly bound to Hb
CO2 Transport
• dissolved in plasma
–7%
• transported as HCO3 (bicarbonate ion)
–70%
• bound to HB
–23%
–attaches to –NH2 groups (amino) of
histidine
–Carbaminohemoglobin HB-CO2
Transport as HCO3
• converted to carbonic acid
– unstable
– dissociates to hydrogen &
bicarbonate ions
• HCO3- diffuses from RBCs
into plasma
• exchanges one HCO3- for
one Cl– chloride shift
– maintains electrical
neutrality
AT LUNG
AT TISSUES
Control of Respiration
• normally cellular rates of absorption &
generation of gases are matched by
capillary rates of delivery & removal
• rates are identical to rates of O2 absorption
& CO2 excretion at lungs
• if absorption & excretion become
unbalanced
– homeostatic mechanisms restore equilibrium
• changing blood flow & O2 delivery
– locally regulated
• changing depth & rate of respiration
– respiratory centers in brain
Respiratory Centers in Brain
• usually breath without
conscious thoughtinvoluntary
– depends on repetitive
stimuli from brain
• automatic, unconscious
cycle of breathing controlled
by respiratory centers in
medulla & pons
• medullary rhymicity area
• pneumotaxic center
• apneustic center
Medullary Rhymicity Center
• controls basic rhythm of respiration
• has an inspiratory & expiratory
area
• nerves project to diaphragm by
phrenic nerve & to intercostals
by intercostal nerves
• quiet breathing
• neuron activity increases for 2 sec.
stimulates inspiratory muscles
• rib cage expands as diaphragm
contracts
– inhalation occurs
• output ceases abruptly muscles
relaxelastic parts recoil
exhalation (lasts 3 seconds)
• neurons begins to fire again
• cycle repeats
Pneumotaxic & Apneustic Centers
•
located in pons
– regulates shift from inspiration to
expiration
•
•
•
•
•
•
•
•
•
•
regulate respiratory rate & depth of
respiration in response to sensory stimuli
or input from other brain centers
pneumotaxic center-upper pons
transmits inhibitory impulses to
inspiratory area
helps turn off inspiratory area before
lungs become too full of air
increased pneumotaxic output quickens
respiration by shortening duration of each
inhalationbreathing rate increases
decreased outputslows respiratory pace
depth of respiration increases
apneustic center sends stimulating
impulses to inspiratory area
activates it producing prolonged
inhalation.
result is long, deep inhalations
Regulation of Respiratory Centers
• conscious or voluntary
control
• inhale or exhale at will
• input form cerebral motor cortex
stimulates motor neurons to
stimulate respiratory muscles
bypassing medulla centers
• limited-impossible to override
chemoreceptor reflexes
• nerve impulses from
hypothalamus & limbic system
also stimulate respiratory center
• allows emotional stimuli to alter
respiration
Respiratory Reflexes
• brain centers regulate respiratory rate & depth
of respiration
– in response to sensory stimuli or input from other
brain centers
•
•
•
•
•
•
sensory information comes from
central chemoreceptors
peripheral chemoreceptors
proprioceptors
stretch receptors
information from these alters patterns of
respiration
• changes are respiratory reflexes
Chemoreceptors
• central
chemoreceptors
• neurons in brainstem
that respond to changes
in pH of cerebrospinal
fluid
• stimulation increases
depth & rate of
respiration
• peripheral
chemoreceptors
– carotid & aortic bodies
of large arteries
– respond to PCO2, pH
& PO2 of blood
Respiratory Reflex-CO2
• Hypercapnia
– increase in PCO2
• CO2 crosses blood brain
barrier rapidly
• rise in arterial PCO2 almost
immediately elevates CO2
levels in CSFpH decreases
excites central
chemoreceptors stimulates
respiratory centers increases
depth & rate of breathing
• rapid breathing moves more air
in & out of lungsalveolar CO2
decreases accelerates
diffusion of CO2 out of alveolar
capillaries homeostasis
restored
• results in hyperventilation
Chemoreceptor Reflexes-CO2
• hyperventilation
hypocapnia
– low PCO2
• central & peripheral
chemoreceptors are
not stimulated
• Inspiratory center sets
its own pace
• CO2 accumulates
• homeostasis restored
Stretch Receptors
• found in smooth
muscles of bronchi
& bronchioles & in
visceral pleura
• lung inflation
• signal inspiratory &
apneustic areas via
vagus nerve
• Inhibits both
• Hering-Breuer
Reflex